Uncontrolled intracranial hypertension accounts for 50% of all deaths in severely head injured patients. Among survivors, recent data from the Traumatic Coma Data Bank has shown that sustained levels of high ICP result in greater long term disability. Al- though raised ICP remains as the most frequent cause of death and neurologic deficit, the sequence ce of events leading to intracranial hypertension is poorly understood progress has been made in isolating the contribution of CSF add vascular factors to raised ICP. Having established from clinical studies that cerebrospinal fluid (CSF) parameters play a relatively minor role, we now hypothesize that raised ICP is caused predominately by a vascular mechanism. This research seeks to further identify the nature of this vascular mechanism and' show how it interacts with brain tissue pressure to result in raised ICP. Secondly, as ICP is exacerbated by brain swelling, we will seek to identify which process, edema production or vascular engorgement, is responsible for increase in brain bulk using non-invasive magnetic resonance technology. Thirdly, we will extend our studies in gauging the effect of mannitol treatment in improving volume/pressure status in head injured patients to better understand why the ICP reduction is not sustained. Finally, we will apply new techniques to assess cerebral vessel responsivity to test if the marked impairment of vessel reactivity observed in patients is improved with superoxide dismutase (SOD). We view these studies as essential for the identification of mechanisms responsible for raised ICP and the development of more effective means of ICP management for r improvement of patient outcome.